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Asthma Alleviation by Ginsenoside Rb1 via Promotion of Treg Proliferation and Inflammatory T Cell Inhibition
Susanna Choi1, Seung-Ah Yoo2, Kon-Young Ji1
1KM Convergence Research Division, Korea Institute of Oriental Medicine, Daejeon, Republic of Korea.
Allergy
|April 19, 2025
Summary
Ginsenoside Rb1 (gRb1) enhances regulatory T cells (Tregs) and suppresses inflammatory T cells, offering a novel therapeutic strategy for asthma. This natural compound shifts the immune balance, alleviating asthma symptoms by boosting Treg activity.
Area of Science:
- Immunology
- Pharmacology
- Respiratory Medicine
Background:
- Regulatory T cells (Tregs) show therapeutic potential for inflammatory diseases like asthma.
- Current asthma treatments lack agents specifically designed to upregulate Tregs.
- Tregs play a crucial role in regulating inflammation relevant to asthma prognosis.
Purpose of the Study:
- To investigate the potential of natural products for Treg-based asthma therapy.
- To evaluate the effects of ginsenoside Rb1 (gRb1) on Treg and T-cell populations in asthma.
- To explore gRb1 as a novel therapeutic agent for asthma management.
Main Methods:
- Screened a library of 250 natural products to identify Treg-modulating compounds.
- Utilized flow cytometry and cytokine analysis to assess gRb1 effects in mouse asthma models and human PBMCs.
- Evaluated gRb1's impact on Treg and Th17 populations, and T-cell activation markers.
Main Results:
- Ginsenoside Rb1 (gRb1) increased regulatory T cell (Treg) populations and IL-10/TGF-β expression.
- gRb1 decreased pro-inflammatory Th17, Th1, and Th2 cell counts in asthma models.
- gRb1 treatment modulated T-cell activation and differentiation, inhibiting inflammatory cytokine secretion.
Conclusions:
- Ginsenoside Rb1 (gRb1) alleviates asthma symptoms by rebalancing Treg and inflammatory T cells.
- gRb1 enhances Treg activity and differentiation, offering a potential therapeutic strategy.
- These findings suggest gRb1 as a novel treatment for asthma and related inflammatory disorders.
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